Cancer progression is a complex process involving host-tumor interactions through multiple molecular and cellular factors of the tumor microenvironment. In mice, the immune cells appear to prevent the development of tumors and inhibit tumor progression (1). However, through inflammation-dependent mechanisms, the innate immune system can promote tumor development (2, 3). In humans, lymphocytes have been shown to participate in antitumoral responses. Tumor-infiltrating T cells are associated with improved clinical outcome and survival in colorectal cancer patients (4). Similar results were found in breast (5, 6) and lung cancer (7-11).
It was previously shown that a high intratumoral memory T cell density correlated with the decrease of early metastatic events and the prevention of relapse in colorectal cancer patients (12). Furthermore, it was demonstrated that the functional orientation, density and location of immune cells profoundly influence the clinical outcome of patients, regardless of cancer stages (4). In contrast to patients with metastasis or a low density of immune cells, a functional coordination of the immune response was observed in patients without metastasis and with a high density of immune cells (13).